Abstract: The clinical manifestation (including glaucomatous optic nerve damage and visual field damage) and pathogenesis of normal tension glaucoma are in some degree different from primary open angle glaucoma. In this review, the hypothesis of normal tension glaucoma pathogenesis is divided into different subgroups, including hypoxia ischemia subgroup (a link with arterial hypotension, myocardial ischemia, headache and migraine, increased plasma levels of endothelin-1, increased platelet aggregation, or ischemia encephalopathy, etc), abnormal autoimmunity subgroup (with monoclonal gammopathy, anti-rhodopsin antibody, autoantibodies to Heat Shock Proteins , neuron-specific enolase autoantibodies, or antiphospholipid antibodies), neurodegenerative diseases related subgroup (Alzheimer disease, Parkinson disease), abnormal endocrinological subgroup(e.g., hypothyroidism). The hypothesis of normal tension glaucoma pathogenesis subgroups will benefit for the clinical management. (Ophthalmol CHN, 2012, 21: 19-23)

Key words: normal tension glaucoma/pathogenesis, normal tension glaucoma/ pathophysiology